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CLINICAL REPORT

Atopic Dermatitis: Skin-Directed Management

abstractAtopic dermatitis is a common inammatory skin condition character-

ized by relapsing eczematous lesions in a typical distribution. It can be

frustrating for pediatric patients, parents, and health care providers

alike. The pediatrician will treat the majority of children with atopic

dermatitis as many patients will not have access to a pediatric medical

subspecialist, such as a pediatric dermatologist or pediatric allergist.

This report provides up-to-date information regarding the disease and

its impact, pathogenesis, treatment options, and potential complica-

tions. The goal of this report is to assist pediatricians with accurateand useful information that will improve the care of patients with

atopic dermatitis. Pediatrics 2014;134:e1735–e1744

Atopic dermatitis (AD), commonly referred to as eczema, is a chronic,

relapsing, and often intensely pruritic inammatory disorder of the

skin. A recent epidemiologic study using national data suggested that

the pediatric prevalence is at least 10% in most of the United States.1

AD primarily affects children, and disease onset occurs before the ages

of 1 and 5 years in 65% and 85% of affected children, respectively.1

The number of of ce visits for children with AD is increasing.2 Up to80% of children with AD are diagnosed and managed by primary care

providers, often pediatricians.3 Although medical subspecialists, such

as pediatric dermatologists and/or pediatric allergists, may be suited

to provide more advanced care for children with AD, lack of a suf cient

number of such physicians, particularly pediatric dermatologists,4

likely means the burden of AD care will continue to fall to primary care

providers. Although consensus guidelines and practice parameters

regarding the management of AD in children have been published,5–10

considerable variability persists in clinical practice, particularly re-

garding the roles that bathing, moisturizing, topical medications, and

allergies play in management. Inconsistencies in opinion and treat-ment approach as well as the chronic and relapsing nature of AD can

lead to frustration for the patient, family, and primary care providers

when managing AD.

STATEMENT OF THE PROBLEM

New data support the theory that AD results from primary abnormalities

of the skin barrier,11 suggesting that skin-directed management of AD is

of paramount importance. This clinical report reviews AD and provides

an up-to-date approach to skin-directed management that is based on

pathogenesis. Effectively using this information to create treatment plans

Megha M. Tollefson, MD, Anna L. Bruckner, MD, FAAP, and

SECTION ON DERMATOLOGY

KEY WORDS

atopic dermatitis, eczema, skin care, treatment, topical

corticosteroids

ABBREVIATIONS

ACD—allergic contact dermatitis

AD—atopic dermatitis

IgE—immunoglobulin E

MRSA—methicillin-resistant Staphylococcus aureus

NIAID—National Institute of Allergy and Infectious Diseases

QoL—quality of life

TCI—

topical calcineurin inhibitor

This document is copyrighted and is property of the American

Academy of Pediatrics and its Board of Directors. All authors

have led conict of interest statements with the American

Academy of Pediatrics. Any conicts have been resolved through

a process approved by the Board of Directors. The American

Academy of Pediatrics has neither solicited nor accepted any

commercial involvement in the development of the content of

this publication.

The guidance in this report does not indicate an exclusive

course of treatment or serve as a standard of medical care.

Variations, taking into account individual circumstances, may be

appropriate.

Clinical reports from the American Academy of Pediatrics

bene t from expertise and resources of liaisons and internal

(AAP) and external reviewers. However, clinical reports from the

American Academy of Pediatrics may not reect the views of the

liaisons or the organizations or government agencies that they

represent.

www.pediatrics.org/cgi/doi/10.1542/peds.2014-2812

doi:10.1542/peds.2014-2812

All clinical reports from the American Academy of Pediatrics

automatically expire 5 years after publication unless reaf rmed,

revised, or retired at or before that time.

PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

Copyright © 2014 by the American Academy of Pediatrics

PEDIATRICS Volume 134, Number 6, December 2014 e1735

FROM THE AMERICAN ACADEMY OF PEDIATRICS

Guidance for the Clinician in

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and educate families should help pe-

diatric primary care providers manage

most children with AD, thereby im-

proving patient satisfaction and clinical

outcomes.

CLINICAL FEATURES

The diagnosis of AD is primarily clinical

(Table 1). Major clinical features are a

pruritic and relapsing eczematous der-

matitis in a typical distribution that

changes with age.9 In infancy, the cheeks,

scalp, trunk, and extremities are most

commonly affected. In early childhood,

the exural areas are characteristic,

whereas in adolescents and adults,

hands and feet are typically involved.

Pruritus is a hallmark of AD, which is

often referred to as the “itch that

rashes.” Other features that support

the diagnosis of AD include early age

of onset, personal or family history

of atopy, ichthyosis vulgaris, and/or

xerosis. It is important to exclude other

inammatory skin conditions, such as

contact dermatitis, seborrheic der-

matitis, and psoriasis. Skin biopsies

and laboratory testing are usually

unnecessary and not helpful in making the diagnosis of AD, although they may

be benecial when trying to exclude

conditions that appear similar to AD

(such as those mentioned previously),

particularly in patients whose symp-

toms are not responding to standard

skin-directed care.

EFFECTS ON QUALITY OF LIFEThe effects of AD on the quality of life

(QoL) of patients and their families

cannot be underestimated. Nearly 50%

of children with AD report a severely

negative effect of the disease on QoL.12

Factors that contribute to poor QoL in

AD are fatigue and sleep deprivation

(which directly correlate with itch and

severity of AD), activity restriction, and

depression. Children with severe AD

also tend to have fewer friends andparticipate in fewer group activities

than their peers.13 These children may

be at higher risk of depression, anxiety,

and other mental health disorders.14

AD also has a negative effect on QoL of

caregivers and parents of affected

children.15 Parents of children with

moderate and severe AD spend up to

3 hours per day caring for their chil-

dren’s skin. The most commonly reported

negative effects on parents are lack of sleep (often because of cosleeping),

fatigue, absence of privacy (because

of cosleeping, disrupted sleep of af-

fected children), treatment-related -

nancial expenditures, and feelings of

hopelessness, guilt, and depression.

In fact, the depression rate in mothers

of children with AD is twice as high as

in mothers of children with asthma.16

Appropriate social and community sup-

port resources, such as referral to a

counselor, psychologist, or patient sup-

port groups, such as the National

Eczema Association (www.nationaleczema.

org), can be helpful when QoL issues

are encountered in patients and families

with AD.

PATHOGENESIS

The pathogenesis of AD is complex and

multifactorial. Skin barrier dysfunction,

environmental factors, genetic pre-

disposition, and immune dysfunction all

play a role in its development and are

closely intertwined. In the past, em-

phasis had been placed on T helper cell

dysregulation, production of immuno-

globulin E (IgE), and mast cell hyper-activity leading to the development of

pruritus, inammation, and the char-

acteristic dermatitis.11 Recent discov-

eries, however, have established the

key role of skin barrier dysfunction in

the development of AD.17

The primary function of the skin barrier

is to restrict water loss and to prevent

entry of irritants, allergens, and skin

pathogens. The outermost layer of skin,

called the stratum corneum, is critical to the integrity of the skin barrier, with

the protein laggrin being a key player

in stratum corneum structure and

formation.18 Loss-of-function mutations

(of which more than 40 have been

described) in FLG, which encodes

laggrin, have been implicated in up

to 50% of patients with moderate to

severe AD in some demographic pop-

ulations.17,19 Mutations in FLG are as-

sociated with a two- to threefoldincreased risk of having AD.20

There are several proposed mechanisms

of how laggrin defects contribute to

the development of AD. Inadequate

laggrin production leads to a reduced

ability of keratinocytes to maintain hy-

dration and to restrict transepidermal

water loss, which then leads to xerosis,

which in turn produces pruritus and,

subsequently, AD.21 An inadequate skin

barrier might also allow for the entryof aeroallergens, leading to an in-

ammatory response, causing AD.

Another theory speculates that local

pH may be changed with an altered

skin barrier, leading to the overgrowth

of bacteria, such as Staphylococcus

aureus , which then may trigger an in-

nate immune response, leading to

the development of inammatory skin

lesions. Regardless of the mechanism,

TABLE 1 Clinical Features in AD5,6,9

Major clinical features

Itching/pruritus

Typical dermatitis with a chronic or relapsing

history

Patient or family members with atopy

Typical distribution and age-specic patterns

Minor clinical features

Early age of onsetDry skin/xerosis

Keratosis pilaris

Ichthyosis vulgaris

Lip dermatitis

Hand eczema

Lichenication

Elevated IgE level

Itching on sweating

Recurrent infections

Pityriasis alba

Dermatographism

Eye symptoms: cataracts, keratoconus,

inammation

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this new knowledge reinforces the pri-

mary role of the skin barrier in the

pathogenesis of AD and highlights the

need for skin-directed therapy to repair

or enhance the function of the skin

barrier.

ALLERGIES AND AD

The relationship between AD and food

allergy is complex but likely over-

emphasized. More than 90% of parents

incorrectly believe that food allergy is

the sole or main cause of their child’s

skin disease.22 The resulting focus on

food allergy can result in elimination

diets; potential nutritional concerns,

such as protein or micronutrient mal-

nutrition or deciencies; and mis-

direction of treatment away from the

skin, thereby leading to undertreat-

ment. Effective treatment of the skin

tends to allay parental concern re-

garding food allergy.23

True food-induced AD is rare. The most

common cutaneous manifestations of

food allergy are often IgE-mediated and

consist of acute urticaria, angioedema,

contact reactions, or in some cases, an

increase in AD symptoms.24,25 In thecase that AD is worsened by exposure

to a food allergen, these reactions are

not IgE-mediated but rather delayed-

type hypersensitivity reactions and

usually develop 2 to 6 hours after the

exposure to the food.26

The accentuated role of food allergies

in AD may stem from the observation

that food allergies are prevalent in

patients with AD. The prevalence of

food allergy in all children in the rst 5years of life is approximately 5%.24 In

children with AD, however, the preva-

lence of food allergy is approximately

30% to 40%,25 and up to 80% will have

high food-specic IgE concentrations,

even in the absence of a true food

allergy.27 In addition, patients who

have food allergy often have earlier-

onset and more severe AD, and pa-

tients with early-onset AD have a higher

risk of developing food allergies than

those with later-onset AD.28 However, it is

important to stress that this relationship

is not causative. Rather, the presence of

food allergy predicts a poor prognosis of

severe and persistent AD, but food al-

lergy does not necessarily cause AD.

Recent guidelines set forth by the Na-

tional Institute of Allergy and Infectious

Diseases (NIAID) support this position.

In these guidelines, the NIAID states: “In

some sensitized patients…food aller-

gens can induce urticarial lesions,

itching and eczematous ares, all of

which may aggravate AD” but do not

cause AD. They also state that, in the

absence of documented IgE- or non-

IgE–mediated food allergy, there is“…little evidence to support the role

for food avoidance” in the treatment of

AD.25 Egg allergy may be one excep-

tion, as up to half of infants with egg-

specic IgE may have improvement in

their AD when following an egg-free

diet.29 The NIAID guidelines state that

allergy evaluation (specically to milk,

egg, peanut, wheat, and soy) should be

considered in children younger than 5

years with severe AD if the child haspersistent AD despite optimal man-

agement and topical therapy or if the

child has a reliable history of an im-

mediate cutaneous reaction after in-

gestion of a specic food.

The “atopic march” is the concept that

AD is the rst stop in the progression

to other allergic disorders, such as

asthma and allergic rhinitis.30 It has

been suggested that early optimal and

successful treatment of AD may preventor attenuate the development of other

atopic conditions.31 The recent ndings

of the role FLG mutations play in causing

epidermal barrier defects, thus allowing

for the entry of aeroallergens and other

allergens into the skin and subsequent

epicutaneous sensitization, lends strong

support to this possibility and highlights

the importance of effective skin-directed

treatment of AD.

Allergic contact dermatitis (ACD) is a

delayed hypersensitivity reaction to

cutaneous allergens that is under-

estimated in the pediatric population

and likely plays a greater role in

perpetuating AD than was previously

believed. Up to 50% of children withdif cult-to-control AD have at least 1 pos-

itive patch test reaction to a cutaneous

allergen.32 Not all positive reactions

may be relevant, however. Most studies

estimate 50% to 70% of all positive re-

actions to be relevant in patients with

suspected ACD. Thus, the possibility of

ACD should be considered in children

with unusual or dif cult-to-control AD.

TREATMENT PRINCIPLES

Skin-directed therapies should be the

rst approach to management. This

approach has 4 main components, each

focusing on a specic manifestation of

AD: (1) maintenance skin care, designed

to repair and maintain a healthy skin

barrier; (2) topical antiinammatory

medications, to suppress the inam-

matory response; (3) itch control; and

(4) managing infectious triggers, rec-

ognition and treatment of infection-

related ares. Education of patients

and families is another critical factor

that should not be overlooked. AD is

a frustrating disease because of its

recurrent nature, even in the face of

excellent care plans. When the primary

care provider is able to set realistic

expectations regarding outcomes, pa-

rental compliance is better and frus-

tration is decreased. It can be helpful

to discuss the prognosis of AD, be-cause most children will outgrow the

symptoms or at least the severity of

the disease.27 Patients whose parents

receive comprehensive education re-

garding AD and its care have better

improvement in AD severity than pa-

tients whose parents do not receive

this education.33 Written action plans

have been shown to improve adherence

in children with asthma, and a similar




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model for patients with AD (see Fig 1 for

an example), outlining specic indica-

tions for different products and medi-

cations, is likely to be helpful.34,35

Maintenance Skin Care

Maintenance skin care is the founda- tion of AD management; its goal is to

repair and maintain a functional skin

barrier. Patients should be instructed

to develop these habits and perform

them daily. Preliminary evidence sup-

ports the role of maintenance skin

care in helping to reduce both the

frequency and severity of AD ares.

The key facets of maintenance care

include maintaining skin hydration

and avoiding irritants and triggers.

The optimal frequency of bathing for

children with AD has not been well

studied and remains controversial.

Soaking baths allow the skin to imbibe

moisture, and a daily bath can be

benecial in patients with AD as long

as a moisturizer is applied after-

ward.30,36 The specic frequency of

bathing should be titrated to theindividual patient and his or her

response to bathing. The use of

lukewarm water and limiting the

duration of the bath can prevent skin

dehydration. Cleansing may also re-

move bacteria from the skin surface.

A mild synthetic detergent without

fragrance can be used to cleanse

soiled areas without fear of exac-

erbating the skin disease. Additives

are not proven to be effective, although dilute bleach can be helpful

for patients who are prone to infection

and ares (see Managing Infectious

Triggers).

A second and extremely important

component of maintaining skin hydra-

tion is lubrication of the skin, commonly

referred to as moisturization. Frequent

moisturization alleviates the discomfort

associated with xerosis, helps to repair

the skin barrier, and reduces the quan-

tity and potency of pharmacologic inter-

ventions.37,38 In a British study evaluating

51 children with AD, parents were ed-

ucated on the proper use of moistur-

izers and topical treatments by a nurse

specialist. During the study period, the

quantity of moisturizer used increased

800% (average use of 426 g per week

per patient) while the severity of ADdecreased and the percentage of pa-

tients having to use moderate or po-

tent topical steroids decreased.39

Studies comparing the relative effec-

tiveness of specic moisturizers are

lacking, and the plethora of products

can make the task of choosing a

moisturizer daunting. Simplistically,

all moisturizers are mixtures of lipid

(liquid or semisolid) and water. Oint-

ments have the highest proportion of lipid (for example, petroleum jelly is

100% lipid) and likewise feel “greasy”

when applied to the skin. Creams are

emulsions of water in lipid (oil>water)

and contain preservatives and stabi-

lizers to keep these ingredients from

separating. Although creams can be

less greasy than ointments, the added

ingredients can sometimes burn or

sting atopic skin. Similarly, lotions are

also emulsions with a higher pro-portion of water to lipid than creams.

Frequent reapplication of lotions is

needed to maintain skin hydration. In

general, ointments tend to have the

greatest moisturizing effect, followed

by creams, and then lotions. The best

moisturizers for patients with AD are

fragrance free and have the least

possible number of preservatives, be-

cause these are potential irritants.FIGURE 1

An action plan for the management of AD.


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Moisturizers should be applied at least

once daily to the entire body, regard-

less of whether dermatitis is present.

There are a handful of prescription bar-

rier creams marketed for the treat-

ment of AD. These products do not have

active pharmacologic ingredients. A smallstudy compared 2 of these products

with an over-the-counter ointment and

revealed no signicant difference in ef-

cacy for patients with mild-to-moderate

AD, as dened by investigator global

assessment.40 Although no major ad-

verse effects have been reported with

these products, they are considerably

more expensive and may, therefore,

be less cost effective than standard

moisturizers.Multiple patient-specic factors, com-

monly referred to as triggers, may

exacerbate AD. Triggers may be un-

avoidable, but minimizing exposure to

them can be helpful. Common triggers

may include aeroallergens or environ-

mental allergens, infections (particu-

larly viral illnesses), harsh soaps and

detergents, fragrances, rough or non-

breathable clothing fabrics, sweat, ex-

cess saliva, and psychosocial stress.

Topical Antiinammatory

Medications

The eczematous dermatitis seen in AD

is the manifestation of an inam-

matory immune response in the skin.

Flares of dermatitis are unlikely to

respond to moisturization alone, and

during these times, treatment is fo-

cused on suppressing the inam-

matory response. Topical steroids are the rst-line, most commonly used

medications to treat active AD and

have been used for the last 40 to 50

years.30 When used appropriately, they

are effective and safe.41 However,

when used inappropriately, there are

potential risks of cutaneous atrophy,

striae, telangiectasia, and systemic ab-

sorption with resulting adrenal sup-

pression. There are also other potential

local effects when used around the eyes

(intraocular hypertension, cataracts)

or mouth (perioricial dermatitis). Be-

cause of these potential risks, there is

a real phenomenon of “steroid phobia”

on the part of both parents and health

care providers. Although this phobiadoes not correlate with AD severity, it

does lead to undertreatment of the

skin disease.42,43

Topical steroids are classied accord-

ing to their potency, ranging from class

VII (low potency) to class I (super po-

tent; Table 2). Class I medications are

1800 times more potent than the least

potent class VII medications. Risk of

adverse effects directly correlates with

potency, with high-potency and super-potent topical steroids carrying the

greatest risk. When treating most cases

of AD, high-potency medications are

generally not needed. Patients treated

with higher-potency topical steroids are

at risk for developing the aforemen-

tioned adverse effects, making close

follow-up necessary. Choosing an ap-

propriate topical steroid can be dif-

cult, given the number of different

medications, and health care pro-viders are advised to rely on 2 or 3

medications from the low- (classes VI

and VII) and moderate-potency groups

(classes III, IV, and V) as “go-to” medi-

cations for everyday practice. These

choices may be based on regional

prescribing practices and insurance

coverage or cost. Inexpensive low-

and moderate-potency generic topical

steroids are hydrocortisone and tri-

amcinolone, respectively. Acceptable“limits” of topical steroid potency in a

primary care practice are low-potency

topical steroids for the face, neck,

and skin folds and moderate-potency

topical steroids for the trunk and

extremities.

For acute ares and moderate to se-

vere cases, wet wrap therapy (also

called wet dressings) can be used in

conjunction with topical steroids to

quickly control the dermatitis.44 Wet

dressings increase penetration of top-

ical steroids into the skin, decrease

TABLE 2 Topical Steroid Medications byClass

Class I: Superpotent

Clobetasol propionate 0.05% ointment, cream,

solution, and foam

Diorasone diacetate 0.05% ointment

Fluocinonide 0.1% cream

Halobetasol propionate 0.05% ointmentand cream

Class II: High potency

Betamethasone dipropionate 0.05% ointment

and cream

Budesonide 0.025% cream

Desoximetasone 0.25% ointment and cream

Diorasone diacetate 0.05% cream

Fluocinonide 0.05% ointment, cream, and gel

Halcinonide 0.1% cream and ointment

Mometasone furoate 0.1% ointment

Class III: Moderate potency

Betamethasone valerate 0.1% ointment, foam

Desoximetasone 0.05% cream

Diorasone diacetate 0.05% cream

Fluticasone propionate 0.005% ointment

Triamcinolone acetonide 0.1% ointment

Triamcinolone acetonide 0.5% cream

Class IV: Moderate potency

Betamethasone valerate 0.12% foam

Clocortolone pivalate 0.1% cream

Flurandrenolide 0.05% ointment

Fluocinolone acetonide 0.025% ointment

Halcinonide 0.025% cream

Hydrocortisone valerate 0.2% ointment

Mometasone furoate 0.1% cream and lotion


Class V: Moderate potency

Betamethasone valerate 0.1% cream

Clocortolone pivalate 0.1% cream

Flurandrenolide 0.025% ointment

Flurandrenolide 0.05% cream

Fluocinolone acetonide 0.01% cream

Fluocinolone acetonide 0.025% cream

Hydrocortisone butyrate 0.1% ointment,

cream, and lotion

Hydrocortisone probutate 0.1% cream

Hydrocortisone valerate 0.2% cream

Prednicarbate 0.1% cream

Triamcinolone 0.025% ointment

Class VI: Low potency

Alclometasone dipropionate 0.05% ointment

and cream

Desonide 0.05% ointment, cream, lotion,

hydrogel, and foamFluocinolone acetonide 0.01% oil

Flurandrenolide 0.025% cream


Class VII: Low potency

Hydrocortisone 0.5% and 1% ointment

and cream (over the counter)

Hydrocortisone 2.5% ointment, cream,

and lotion




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itch, and serve as an effective deter-

rent to scratching. The technique is

straightforward: after a soaking bath,

topical steroid is applied to affected

areas followed by application of mois-

turizer to the rest of the skin; moist

gauze or cotton clothing that has beendampened with warm water is then

applied; the wet layer is covered with

dry cotton clothing. Blankets and a

warm room keep the child comfort-

able. The dressings can be left in place

for 3 to 8 hours before being changed.

Wet dressings can be used continu-

ously for 24 to 72 hours or overnight

for up to 1 week at a time.

Another consideration when prescrib-

ing topical steroids is the vehicle orform of product by which the active

ingredient is delivered. Ointments are

less likely to produce a burning or

stinging sensation and are better tol-

erated by infants and younger children.

When comparing the same active in-

gredient and concentration, ointments

are more effective than creams or

lotions, because their occlusive effect

results in a higher relative potency.

Topical steroids should be applied asa thin layer once or twice daily to af-

fected areas until these areas are

smooth to touch and no longer red or

itchy. Traditionally, topical steroids are

held when dermatitis is quiescent and

restarted when the eruption recurs.

Placing an absolute limit on the dura-

tion of topical steroid use can be

confusing for families, leads to un-

satisfactory outcomes, and conicts

with the relapsing nature of the diseaseitself. However, if AD is not responding

after 1 to 2 weeks of treatment, re-

evaluation to consider other diagnoses

or treatment plans is indicated. When

these general guidelines are followed,

the risk of adverse effects from the use

of topical steroids is extremely low.

Topical calcineurin inhibitors (TCIs) are

a newer treatment of AD. These medi-

cations are topical immunosuppressive

agents that inhibit T-cell function.

There are currently 2 forms: tacrolimus

ointment (available in 0.03% and 0.1%)

and pimecrolimus 1% cream. Both are

approved as second-line therapy for

moderate-to-severe AD. A recent meta-

analysis in pediatric patients with ADdemonstrated that both tacrolimus and

pimecrolimus are effective; tacrolimus

is more effective than pimecrolimus,

but both reduce the inammation and

pruritus associated with AD.45

TCIs have a different adverse effect

prole than topical steroids and do not

cause atrophy, striae, telangiectasia, and

adrenal suppression. Thus, they are

highly benecial to treat AD in patients

for whom concerns for adverse effectsfrom long-term use of topical steroids are

highest (eg, face, eyelids). The negatives,

however, are a higher relative cost and

the potential adverse effects of burning

and stinging (tacrolimus>pimecrolimus).

In addition, the Food and Drug Adminis-

tration has issued a so-called “black

box” or boxed warning for TCIs, citing

a potential cancer risk with the medi-

cation, on the basis of the observation

that laboratory animals exposed to highdoses of systemic calcineurin inhibitors

developed malignancies more frequently

and on rare case reports of adult pa-

tients using TCIs who developed lym-

phoma and skin cancers.46 However, the

cause-and-effect relationship between

TCI use and malignancy in these case

reports is unclear. Reassuringly, TCIs have

been used in children for more than 15

years, there have been no reports of

malignancy in children, and there is little

to no concern for systemic absorption

or systemic immunosuppression.47

Indeed, in 1 adult study, there was a

lower rate of nonmelanoma skin can-

cer in patients with AD who used TCIs

to treat their inammatory disease.48

Proactive Treatment

Although traditional AD management

consists of treating active disease and

ares with topical steroids and/or TCIs,

emerging data suggest that use of

these medications when a patient is not

having active disease may be helpful

as well. In 1 study, patients used twice-

daily antiinammatory medications to

treat active AD and were then randomly

assigned to receive “proactive”

twice-weekly treatment with topical tacrolimus

or placebo. Patients who received top-

ical tacrolimus had signicantly less

AD ares and increased time to new

are development when compared with

those who received placebo.49 A sim-

ilar effect may also be true with top-

ical steroids (uticasone propionate

and methylprednisolone aceponate have

been studied),50 although none of these

studies have evaluated the long-termsafety of this treatment regimen. The

choice of medication used for are

prevention may depend on patient age,

location of involvement, and cost.

Itch Control

Pruritus is another important com-

ponent of AD. AD is commonly referred

to as the itch that rashes; the asso-

ciated pruritus may be signicant,

even in the absence of signicant rash.

Often, parents may be unaware of howmuch their child scratches, because

itching is generally worse at night. The

pathophysiology behind pruritus is

complex, and both peripheral and

central factors are involved.51 Exam-

ples of peripheral factors are irritant

entry through a defective epidermal

barrier, transepidermal water loss,

and protease activity in the skin.52

Centrally, there is a complex interplay

of multiple different mediators, although histamine seems to have

a limited role, if any.52,53 Clinical fac-

tors can also promote itch, including

scratching (the “itch-scratch” cycle),

xerosis, psychological stress, sweat,

and contact with irritants such as wool

and aeroallergens.

It is often challenging to remove itch,

even when a patient’s skin is improving.

Management of itch initially focuses on


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minimizing triggers and continuing the

skin-directed treatments of restoring the

skin barrier and suppressing inam-

mation. Adjunctive systemic therapy can

be added to help manage itch. Oral

antihistamines do not have a direct ef-

fect on the dermatitis, but can help re-duce the sensation of itching and,

thus, decrease scratching and trauma

to the skin in patients with AD

ares.54 Sedating antihistamines (such

as diphenhydramine or hydroxyzine)

should be used with caution in infants,

who may be more prone to adverse

effects of these agents. In addition,

paradoxical effects of agitation instead

of sedation may occur in some children.

Nonsedating antihistamines (such ascetirizine and loratadine) are less effec-

tive on pruritus but can be helpful for

patients who have environmental allergic

triggers.54 Topical antihistamines are

not effective in the treatment of AD-

associated pruritus and contain poten-

tial irritants and allergens that may

worsen dermatitis.

Managing Infectious Triggers

Both bacterial and viral skin infectionsare associated with ares in children

with AD. Affected patients, particularly

those with poorly controlled AD, have

a higher risk of cutaneous infections.

The skin of patients with AD has an

abnormal expression of antimicrobial

peptides responsible for responding to

bacteria or skin barrier compromise,

toll-like receptor defects, and immune

dysregulation in the form of diminished

immune cell recruitment.55 This com-bination of factors puts patients with

AD at higher risk of skin infection.

Ninety percent of patients with AD are

colonized with S aureus .56 Pruritus

may occur even in patients who are

colonized but not actively infected.

Many patients with AD have sudden

exacerbations of their disease that can

be attributed to active infection with

bacteria, most commonly S aureus ,

and active treatment of the infection

subsequently improves the skin.56 Clin-

ical signs of infection, such as pustules,

oozing and honey-colored crusts, and

less commonly fever and cellulitis, may

lead the primary care provider to

prescribe antibacterial treatment. Sec-ondary infection of AD is a clinical

diagnosis and is often associated with

are of the underlying AD. Obtaining

skin cultures, particularly of pustules

and draining lesions, before treat-

ment can be helpful in determining

the causative pathogen but is not al-

ways necessary. The rate of methicillin-

resistant S aureus (MRSA) colonization

in patients with AD varies depending

on the community in which the patient resides.57 Streptococcal infec-

tions may also occur in patients with

AD. Signs of streptococcal infection

include pustules, painful erosions, and

fever. In addition, patients may have

facial or periorbital involvement and

invasive infections.58

There are multiple synergistic com-

ponents involved in treating active S

aureus and streptococcal infection in

AD. Topical, oral, or intravenous anti-biotic therapy may be needed depend-

ing on the extent and severity of

infection. The specic medication used

should be directed at S aureus and

Streptococcus . Topical mupirocin can

be used for limited skin lesions.

Cephalexin is a common rst-choice

when oral antibiotics are needed and

MRSA is not suspected. Repair of the

skin barrier is continued simultaneously:

bathing, moisturization, and topical anti-inammatory therapies are all usually

indicated. MRSA or other etiologies may

be considered in patients who remain

refractory to treatment.

Dilute bleach baths may have a useful

role in the management of patients

with AD, particularly those prone to

recurrent infection and AD ares. A

recent placebo-controlled, blinded study

examined the effects of 0.005% bleach

baths plus intranasal mupirocin versus

placebo in children with moderate to

severe AD. Patients bathed for 5 to 10

minutes twice weekly with the in-

tervention. Those in the treatment

group had signicant improvement in

their AD severity scores versus thosein the placebo group.56 Areas of the

body that were not submerged in the

bleach-containing water, specically

the head and the neck, revealed no

difference in AD severity scores be-

tween the 2 groups. The treatment was

well tolerated, without any adverse ef-

fect, and without any increase in re-

sistant strains of S aureus . Although

a relatively small study, the results

provide support for the practice of using dilute bleach baths as one mo-

dality in the treatment of patients with

AD. A concentration of 0.005% bleach is

made by adding 120 mL (1/2 cup) of

6% household bleach to a full bathtub

(estimated to be 40 gallons) of water.

The amount of bleach should be ad-

justed based on the size of the bathtub

and the amount of water in the tub.

Patients with AD are also at greater

risk of viral skin infections. These in-clude molluscum contagiosum, eczema

herpeticum, the recently described

atypical enteroviral infection attrib-

utable to Coxsackie virus A6 (the so-

called “eczema coxsackieum”),59 and

vaccinia virus (the virus used in

smallpox vaccine). Patients with eczema

herpeticum present with shallow,

“punched-out” erosions in areas of skin

affected with or prone to AD. Similarly,

the lesions seen with hand, foot, andmouth disease caused by Coxsackie

virus A6 tend to localize to AD skin. In

cases in which the diagnosis is not

clear, viral studies are indicated.

Eczema herpeticum can be potentially

life threatening and requires systemic

treatment with acyclovir. In addition,

adequate analgesia, skin care, and

topical antiinammatory medications

are used. Secondary bacterial infection




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often coexists with eczema herpeticum

and should be treated appropriately as

well. Herpetic keratitis is associated

with periocular eczema herpeticum.60

Smallpox vaccine uses a live vaccinia

virus, and its use was resumed by the

military in 2002. Although it is con- traindicated for those with AD and in

those who have a close contact with

AD, rare cases of eczema vaccinatum

have been reported. Eczema vaccinatum

manifests as a rapidly developing pap-

ular, pustular, or vesicular eruption

with a predilection for areas of AD,

following inadvertent transmission of

vaccinia virus from the unhealed in-

oculation site of the immunized person

to a close contact with AD. Systemicdissemination may follow, and case

fatality rates range from 5% to 40%. If

eczema vaccinatum is suspected, infec-

tious disease experts should be con-

sulted, because treatment with cidofovir

may be necessary.61

Final Points

Using this information, the pediatric

primary care provider should be well

equipped to treat most children withAD. If patients with suspected AD do not

respond to these treatments, referral

to a pediatric medical subspecialist,

such as a pediatric dermatologist, may

be useful. Other reasons for referral

include poorly controlled or gen-

eralized AD with consideration for

systemic immunosuppressive therapy,

recurrent infections (viral or bacterial)in the setting of AD, suspected ACD, and

the presence of atypical features or

physical examination ndings. In cases

of persistent, refractory, and/or gen-

eralized AD, systemic treatment, such

as phototherapy or immunosuppres-

sive medications, may be indicated. Oral

steroids are generally not indicated

because of their adverse side effect

prole and a high likelihood of rebound

dermatitis, making ongoing manage-ment dif cult.

SUMMARY

AD can be a challenging and frustrating

chronic disease for pediatric patients,

parents, and primary care providers.

Although the pathogenesis of AD is

complex, recent research advances

support the role of an abnormal skin

barrier. The clinical corollary to these

discoveries is a greater focus on skin-directed therapies as the rst-line

treatm ent of chi ldren wit h AD. Thi s

includes maintenance skin care and

the use of topical ste roi ds for a cti ve

disease. Low- and moderate-potency

top ical steroi ds are safe and effec-

tive for chi ldren when use d appro-

priately. Early recognition and treatment

of infectious complications can lead toimproved patient outcomes. Patient

and family education and counseling

by the health care provider regarding

the pathogenesis, specic treatment,

and prognosis of the disease play an

extremely important role in the man-

agement of AD.

SECTION ON DERMATOLOGY

EXECUTIVE COMMITTEE, 2013–2014

Bernard A. Cohen, MD, FAAP, Chairperson

Richard Antaya, MD, FAAP

Anna Bruckner, MD, FAAP

Kim Horii, MD, FAAP

Nanette B. Silverberg, MD, FAAP

Teresa Wright, MD, FAAP

FORMER EXECUTIVE COMMITTEE

MEMBERS

Sheila Fallon Friedlander, MD, FAAP

Albert Yan, MD, FAAP

EX OFFICIO

Michael L. Smith, MD, FAAP

STAFF

Lynn M. Colegrove, MBA

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